Search PubMed⌕ Search

Biomedical subjects

A Greenberg

Publications and source records attributed to A Greenberg.

At least 91 records · Page 5Linked to original sources

Chronic effects of nitrendipine on renal hemodynamics and tubular transport.

The effects of nitrendipine (10 mg, during acute clearance experiments) given both acutely and after 2 weeks of administration were examined in normal and hypertensive subjects. At the initiation of therapy, nitrendipine caused an increase in glomerular filtration rate and effective renal plasma flow in the hypertensive, but not in the normal, group. Percentage excretion rates of sodium (%ENa) and phosphate (%EPi) and free water clearance (CW) increased in both groups at the initiation of therapy. After 2 weeks of nitrendipine therapy repeat acute clearance studies showed that the drug no longer increased glomerular filtration rate or effective renal plasma flow in hypertensive subjects, the increases in %ENa and CW persisted in normal subjects and trended upward in hypertensive subjects, and the increase in %EPi persisted in both normal and hypertensive individuals. We conclude that nitrendipine is not sodium retentive after chronic therapy and the acute increase in %ENa, %EPi, and CW after its initial administration suggests a proximal tubular effect.

Adult↗

Variant of Bartter's syndrome with a distal tubular rather than loop of Henle defect.

A 19-year-old normotensive patient had all of the clinical features of Bartter's syndrome: hypokalemia, elevated renin and aldosterone levels and increased excretion of prostaglandin E. In contrast to the patients described by Bartter, the patient had a normal capacity to form solute-free water, suggesting intact loop of Henle function. Baseline potassium and chloride excretion rates were higher than those observed in 5 normal subjects, but the response to intravenous chlorothiazide, a drug which acts in the early distal convolute tubule, was abnormal. While chloride excretion rose by only 61% in this patient, it increased sixfold in the normal subjects. Sodium excretion quadrupled in the controls but less than doubled in this patients. Roughly equivalent increments in potassium excretion occurred in normals and controls, suggesting that the patient's distal potassium-secretory mechanism was intact. Review of the literature indicates that whether the site of the abnormal renal tubular potassium (chloride) leak is the proximal tubule, the loop of Henle or the distal convoluted tubule, patients may achieve features indistinguishable from those previously reported as characteristic for Bartter's syndrome. If loop of Henle malfunction is required to diagnose classical Bartter's syndrome, then our patient (and several reported elsewhere) has a variant form.

Adult↗

Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure.

It has been postulated that hyperparathyroidism in chronic renal failure results from hypocalcemia, occurring, in part, from phosphate retention and/or deficient 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] synthesis. However, many studies have failed to demonstrate hyperphosphatemia or low 1,25-(OH)2D levels in patients with mild renal failure. We measured creatinine clearance (CCr), fractional excretion of phosphorus (FEP), and serum phosphorus, ionized calcium, and plasma N-terminal PTH, and 1,25-(OH)2D concentrations in 21 normal subjects and 51 patients with renal failure. Patients with mild renal failure (Ccr, greater than 40 mL/min.1.73 m2) had normal mean serum phosphorus and ionized calcium and decreased mean 1,25-(OH)2D levels compared with those in normal subjects. In patients with moderate renal failure (CCr, 20-40), the mean ionized calcium level was normal, plasma PTH levels and FEP were elevated, and the decrement in 1,25-(OH)2D was more pronounced. The mean ionized calcium level was decreased only in the group of patients with severe renal failure (CCr, less than 20). The 1,25-(OH)2D values correlated positively with CCr and negatively with the log of plasma PTH and serum phosphorus concentrations. Log of plasma PTH correlated negatively with CCr and positively with FEP. The ionized calcium concentration correlated very weakly with CCr and the log of the plasma PTH level. These data demonstrate the presence of hyperparathyroidism, normocalcemia, and 1,25-(OH)2D deficiency in renal failure and are consistent with a role for 1,25-(OH)2D in the suppression of parathyroid activity through as yet unidentified mechanisms.

Adult↗

Hypercalcemia. A complication of advanced chronic liver disease.

Hypercalcemia has not previously been recognized as a complication of advanced chronic liver disease without hepatoma. During a five-year period, 16 patients evaluated in the liver transplantation program at the University of Pittsburgh developed hypercalcemia. All had advanced chronic liver disease with mean total bilirubin concentration of 29.5 +/- 4.6 mg/dL (50.1 +/- 78.2 mumol/L) (mean +/- SEM) and prothrombin time 16.8 +/- 0.8s. The highest serum calcium level was 17.2 mg/dL (4.3 mmol/L). The mean serum calcium level was 11.7 +/- 0.3 mg/dL (2.93 +/- 0.075 mmol/L) with an ionized calcium level of 5.41 +/- 0.35 mg/dL (1.35 +/- 0.088 mmol/L) and a phosphorus level of 4.2 +/- 0.4 mg/dL (1.4 +/- 0.1 nmol/L). Mild to moderate renal insufficiency was present in 14 (87%) patients; the mean serum creatinine level was 2.8 +/- 0.4 mg/dL (247 +/- 35 mumol/L). In five (38%) patients parathyroid hormone was completely suppressed and in an additional five (38%) patients, it was in a range most compatible with nonhyperparathyroid hypercalcemia. The 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D levels were normal or low in the 11 patients in whom determinations were made. Hypercalcemia that is not due to hyperparathyroidism or hypervitaminosis D is a potential complication of advanced chronic liver disease.

Adult↗

Early and late forms of cyclosporine nephrotoxicity: studies in cardiac transplant recipients.

To characterize the two forms of cyclosporine nephrotoxicity, we examined renal function in the immediate and late postoperative periods after cardiac transplantation. Moderate azotemia occurred during the first postoperative week in 58% of 43 cyclosporine-treated recipients, but in only 34% of 41 azathioprine-treated recipients, and 4% of 25 patients undergoing cardiopulmonary bypass for nontransplant surgery (both P less than .01 v cyclosporine). Acute renal failure developed in an additional 12% of the cyclosporine-treated group. Late postoperative renal dysfunction also occurred with a high prevalence. Life-table analysis indicated that at 6 months 55%, at 12 months 17%, at 24 months 4%, and at 36 months no cyclosporine-treated recipients retained normal renal function. Three renal biopsies performed in subjects with late nephrotoxicity demonstrated prominent interstitial fibrosis. Although one patient subsequently required chronic dialysis, reduction of cyclosporine dosage from a mean of 5.3 +/- 0.7 mg/kg/d to a mean of 2.3 +/- 0.3 mg/kg/d 9 to 21 months after transplantation with concurrent initiation of azathioprine therapy to prevent rejection led to an improvement of renal function in the five patients so treated. These data indicate that there are two distinct forms of cyclosporine nephrotoxicity. Although both occur with high prevalence, the early form does not appear to be a specific risk factor for the late form.

Acute Kidney Injury↗

Extinction of expression of immunoglobulin genes in myeloma X fibroblast somatic cell hybrids.

Adherent hybrids between immunoglobulin-producing mouse myeloma cells and fibroblasts do not produce immunoglobulin polypeptide chains. These hybrids retained the actively rearranged immunoglobulin genes of the myeloma parental cells but lacked immunoglobulin heavy- and light-chain RNA transcripts. We conclude that the shutoff of immunoglobulin production in these hybrids occurs at the transcription or early processing level.

Animals↗

Evaluation of a clinical case definition of AIDS in African children.

In July 1986, a provisional clinical case definition of AIDS in children, developed by the World Health Organization (WHO) for surveillance purposes in Africa, was tested on 159 patients hospitalized in the Department of Pediatrics at Mama Yemo Hospital, Kinshasa, Zaire. Twenty-one (13%) of these children were seropositive for HIV. In this population, the clinical case definition of pediatric AIDS was found to be fairly specific (87%) but lacked sensitivity (35%). The positive predictive value for HIV seropositivity was 25%. This study suggests that it is more difficult to define AIDS clinically in children than in adults and that the utility of the proposed WHO clinical case definition for pediatric AIDS for surveillance of children's AIDS in Africa is limited.

Acquired Immunodeficiency Syndrome↗

In vivo bone lead measurements: a rapid monitoring method for cumulative lead exposure.

Lead concentrations (microgram/g wet weight) in human bone (tibia) were measured noninvasively in vivo employing an X-ray fluorescence technique. Forty-five workers who had been subjected to chronic industrial exposure were found to have a mean bone lead content of 52.9 micrograms/g wet weight (0 to 198 micrograms/g). In addition to bone lead content, blood lead, body burden of lead as assessed by urinary lead excretion after EDTA chelation, zinc protoporphyrin, and unstimulated urinary lead excretion were evaluated. The results suggest that the in vivo measurement of tibia lead content may serve as an acceptable indicator of body lead burden and provide a practical technique for lead screening purposes. The correlation coefficient between X-ray fluorescence findings and lead excretion following Ca-EDTA administration is 0.69; p less than 0.001.

Bone and Bones↗

Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations.

Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.

Adolescent↗

Serum electrolyte patterns in end-stage renal disease.

The charts of 70 successive patients presenting for dialysis therapy for end-stage renal disease (ESRD) were evaluated for their serum electrolyte values. The "classical" pattern of low total CO2 (tCO2), elevated anion gap ("delta"), and normal chloride was found in a minority of patients (14 of 70, or 20%). Hyperchloremia was noted in 46%; in 21 patients (30%), this was associated with a normal delta and in 11 (16%), hyperchloremia was accompanied by an elevated delta. Fourteen patients (20%), most with diabetic nephropathy, had normal serum electrolytes. Patients with chronic glomerulonephritis had a hyperchloremic pattern as often as not, and two of four patients with interstitial nephritis demonstrated hyperchloremia without an elevated delta. We conclude that the previously held thesis that hyperchloremia is a rare or absent finding by the time renal failure progresses to ESRD is no longer tenable. Furthermore, a significant minority of ESRD patients may require the initiation of dialysis at a time when their serum electrolytes are still normal.

Acid-Base Equilibrium↗

Acute renal failure due to high-grade obstruction following therapy with epsilon-aminocaproic acid.

An 18-year-old man with mild factor VIII deficiency developed hematuria and, subsequently, acute renal failure due to high-grade urinary obstruction by clots during therapy with cryoprecipitate, epsilon-aminocaproic acid, and acetazolamide administered for ocular trauma. Discontinuation of therapy with the latter two agents and induction of a brisk diuresis with intravenous (IV) fluid therapy resulted in return of renal function concomitant with spontaneous clot passage. A review of previous literature suggests that hemophiliacs may be more susceptible than nonhemophiliacs to high-grade urinary obstruction due to clot formation when epsilon-aminocaproic acid is administered during episodes of hematuria. Acute flank pain, fever, and delayed dense nephrograms on IV pyelogram are characteristic of the syndrome and distinguish it from other forms of acute renal failure associated with epsilon-aminocaproic acid.

Acute Kidney Injury↗

Cholesterol atheroembolic renal disease. Report of 3 cases with emphasis on diagnosis by skin biopsy and extended survival.

Because antemortem diagnosis is difficult, renal failure due to cholesterol atheroembolism has, until recently, been regarded as a uniformly irreversible and generally fatal disease. Of late, recovery of renal function in several patients in whom the diagnosis was made by organ or other invasive biopsy has been reported. Three cases of cholesterol atheroembolic renal failure in which the diagnosis was made by simple, noninvasive biopsy of the skin in areas showing livedo reticularis are described. Two of the patients, including 1 who required dialysis for 2 months, had an extended survival with recovery of renal function.

Acute Kidney Injury↗

Renal hemodynamic and tubular transport effects of nitrendipine.

Nitrendipine, a 1,4-dihydropyridine derivative, is a new calcium entry blocker with marked antihypertensive effects. Because relatively few data are available regarding its renal effects, we studied the drug's action on renal hemodynamics and electrolyte excretion in normal male volunteers. During sustained water diuresis, 5 to 10 mg nitrendipine given orally caused an increase in urine flow rate and a modest but consistent increase in sodium excretion (from 1.0% to 2.2% of filtered load, P less than 0.01). Furthermore, both solute-free water clearance and percentage of free water excreted rose (from 10.1 +/- 0.6 ml/min to 12.0 +/- 0.8 ml/min and from 8.7% +/- 0.5% to 10.5% +/- 1.1%, respectively, P less than 0.05 in each case). In addition, during the peak effect of the drug on sodium and free water excretion, there was no consistent change in either glomerular filtration rate or effective renal plasma flow. Nitrendipine was also phosphaturic and calciuric but did not alter acid excretion. When administered to subjects with hydropenia receiving hypertonic saline infusion, the drug had no effect on solute-free water reabsorption. We interpret these results to indicate that nitrendipine has direct tubular effects on renal electrolyte transport and that the locus of these effects is probably the proximal tubule. Thus, nitrendipine appears to differ from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.

Administration, Oral↗